Down-regulation of type I Runx2 mediated by dexamethasone is required for 3T3-L1 adipogenesis.

Runx2, a runt-related transcriptional factor family member, is involved in the regulation of osteoblast differentiation. Interestingly, it is abundant in growth-arrested 3T3-L1 preadipocytes and was dramatically down-regulated during adipocyte differentiation. Knockdown of Runx2 expression promoted 3T3-L1 adipocyte differentiation, whereas overexpression inhibited adipocyte differentiation and promoted the trans-differentiation of 3T3-L1 preadipocytes to bone cells.

Transcriptional activation of histone H4 by C/EBPβ during the mitotic clonal expansion of 3T3-L1 adipocyte differentiation.

CCAAT enhancer binding protein β (C/EBPβ) is required for both mitotic clonal expansion (MCE) and terminal differentiation during the 3T3-L1 adipocyte differentiation program. Whereas the mechanism of C/EBPβ during terminal differentiation is well understood, the mechanism of C/EBPβ in MCE is not. We provide evidence that histone H4, the most conserved cell cycle-related histone, the change of which is strictly correlated with DNA content change during the cell cycle, is transcriptionally activated by C/EBPβ during MCE.

Transcription factor YY1 promotes adipogenesis via inhibiting CHOP-10 expression.

CHOP-10, a dominant-negative member of the C/EBP family of transcription factors, is initially expressed by growth-arrested preadipocytes and sequesters/inactivates C/EBPbeta through heterodimerization with its leucine zipper during 3T3-L1 preadipocyte differentiation. Our previous studies indicated that, FBS leads to the down-regulation of CHOP-10 expression after induction, and releasing C/EBPbeta from inhibitory constraint, allowing the transactivation of C/EBPalpha and PPARgamma genes, transcription factors required for terminal adipocyte differentiation. In the present study, we reported that FBS induced the expression of YY1, which bound to CHOP-10 promoter via two adjacent YY1-binding sites, suppressing its expression.

Rehmannia inhibits adipocyte differentiation and adipogenesis.

Rehmannia glutinosa, a Traditional Chinese Medicine (TCM), has been used to increase physical strength. Here, we report that Rehmannia glutinosa extract (RE) inhibits adipocyte differentiation and adipogenesis. RE impairs differentiation of 3T3-L1 preadipocytes in a dose-dependent manner.

Lactacystin inhibits 3T3-L1 adipocyte differentiation through induction of CHOP-10 expression.

Hormonal induction triggers a cascade leading to the expression of CCAAT/enhancer-binding protein(C/EBP)alpha and peroxisome proliferator-activated receptor (PPAR) gamma, C/EBPalpha, and PPARgamma turns on series of adipocyte genes that give rise to the adipocyte phenotype. Previous findings indicate that C/EBPbeta, a transcriptional activator of the C/EBPalpha and PPARgamma genes, is rapidly expressed after induction, but lacks DNA-binding activity and therefore cannot activate transcription of the C/EBPalpha and PPARgamma genes early in the differentiation program. Acquisition of DNA-binding activity of C/EBPbeta occurs when CHOP-10, a dominant-negative form of C/EBP family members, is down-regulated and becomes hyperphosphorylated as preadipocytes traverse the G1-S checkpoint of mitotic clonal expansion.

Identification of a peroxisome proliferator responsive element (PPRE)-like cis-element in mouse plasminogen activator inhibitor-1 gene promoter.

PAI-1 is expressed and secreted by adipose tissue which may mediate the pathogenesis of obesity-associated cardiovascular complications. Evidence is presented in this report that PAI-1 is not expressed by preadipocyte, but significantly induced during 3T3-L1 adipocyte differentiation and the PAI-1 expression correlates with the induction of peroxisome proliferator-activated receptor gamma (PPARgamma). A peroxisome proliferator responsive element (PPRE)-like cis-element (-206TCCCCCATGCCCT-194) is identified in the mouse PAI-1 gene promoter by electrophoretic mobility shift assay (EMSA) combined with transient transfection experiments; the PPRE-like cis-element forms a specific DNA-protein complex only with adipocyte nuclear extracts, not with preadipocyte nuclear extracts; the DNA-protein complex can be totally competed away by non-labeled consensus PPRE, and can be supershifted with PPARgamma antibody.

[Preparation and functional study of an adenovirus vector expressing human plasminogen kringle 5 gene].

Tumor angiogenesis plays a pivotal role in the progress of tumor. Among the various endogenous angiogenic inhibitors discovered, the human plasminogen kringle 5 (K5) has been demonstrated to be a potential inhibitor of the proliferation and migration of vascular endothelial cells in vitro. The replication-incompetent adenovirus (Ad) vector Adeno-X-CMV-K5 (Ad-K5) (where CMV is cytomegalovirus) was constructed and its antiangiogenic effect was tested on vascular endothelial cell and tumor cell.

Glucose and Insulin Regulate Leptin Expression in 3T3-F442A Adipocytes.

Relative quantitation RT-PCR was used to investigate the regulation of leptin expression in 3T3-F442A adipocytes by glucose and insulin. The results showed that glucose and insulin stimulated the expression of leptin in 3T3-F442A adipocytes, but they did not act synergically. Over-high concentration of glucose suppressed the expression of leptin and the effect of insulin.